Electrolyte Imbalances

Sodium range

135-145 mEq/L

Sodium role

ECF concentration and volume, water distribution between ICF and ECF, generating/transmitting nerve impulses, muscle contractility, regulating acid/base balance

What regulates sodium?

kidneys and aldosterone

How does hypernatremia happen?

water loss or sodium gain - inadequate water intake, excess water loss, or rarely sodium gain

Clinical states that cause hypernatremia

diabetes insipidus, nephrogenic diabetes insipidus, inadequate water intake plus increased sodium intake, primary aldosteronism

What happens to cells in hypernatremia?

Fluid shifts OUT of cell into ECF causing cellular dehydration

Hypernatremia clinical manifestations

thirst, lethargy, agitation, seizures, coma, impaired LOC, dry swollen tongue, postural hypotension, weight loss

How do we treat hypernatremia?

treat underlying cause - primary water deficit: increase oral fluids or IV NS, Sodium Excess: dilute sodium with sodium free IV fluids and use diuretics

How fast should sodium levels go down?

Serum Na levels should NOT decrease by more than 8-15mEq/L in an 8 hour period

How does hyponatremia happen?

loss of sodium containing fluids, water excess in relation to sodium, or both

Clinical states that cause hyponatremia

vomiting, diarrhea, NG suction, draining wounds, primary adrenal insufficiency, SIADH, inappropriate use of hypotonic fluids

What happens to the cells in hyponatremia?

Fluid shifts INTO the cells from the ECF leading to cellular edema

clinical manifestations of hyponatremia

headache, irritability, difficulty concentrating, vomiting, confusion, seizures, and coma

How do we treat hyponatremia?

mild (caused by water excess): fluid restriction, acute/and or severe: small amounts of hypertonic 3% saline

How fast should sodium levels increase?

Level should not increase more than 10-12 mEq/L in the first 24 hours

and 18 mEq or less per hour within 48 hours.

What is the normal range for potassium?

3.5-5.0 mEq/L

What is potassium normally used for the in body?

Transmission and conduction of nerve, muscle and cardiac function, regulating intracellular osmolality, acid-base balance

How do we get most of our potassium?

diet - bananas, oranges, prunes, cooked spinach, etc

What is the relationship between sodium and potassium in kidneys?

inverse relationship, when body holds on the sodium, potassium is excreted

What causes hyperkalemia?

renal failure (most common), massive intake, impaired renal excretion, shift from ICF to ECF, salt substitutes and K containing drugs, burns, trauma, intense exercise, metabolic acidosis

Clinical manifestations of hyperkalemia?

weak/paralyzed skeletal muscle, VFid or cardiac standstill, abdominal cramping or diarrhea

What do we see on an EKG for hyperkalemia

tall, peaked T waves, widened QRS, think BIG EKG

How do we treat hyperkalemia?

discontinue oral or parenteral intake, increase elimination of K (diuretics), IV regular insulin and dextrose to shift potassium from ECF to ICF, IV calcium chloride or calcium gluconate (does not lower K!! only stabilizes cardiac membrane)

What should we do when treating hyperkalemia?

continuous ECG, BP monitoring especially if calcium is given, watch for hypoglycemia if giving insulin

What causes hypokalemia?

abnormal loss of K through GI tract or kidneys, diarrhea, misuse of laxatives, vomiting, magnesium deficiency, metabolic alkalosis

Clinical manifestations of hypokalemia?

cardiac changes is most serious, weakness and paresthesia of skeletal muscle, weakness of respiratory muscles, decreased GI motility

What does EKG look like for hypokalemia?

Prominent U wave, flattened T wave, ST depression, think narrow small EKG

How do we treat hypokalemia?

IV KCL but always dilute and rate cannot exceed 10 mEq/hr, never push or bolus,

What should we do for patient on KCl infusion?

Assess IV site hourly for phlebitis, continuous ECG monitoring, urine output and potassium levels

Range for Calcium

9.0-10.5 mg/dL

What is calcium used for in body?

major cation in bones and teeth, blood clotting, nerve impulse transmission, heart and muscle contraction

What is needed for calcium absorption?

active form of vitamin D

What regulates calcium?

Parathyroid hormone: low levels cause release of PTH which increases reabsorption of calcium. Calcitonin: stimulated when calcium levels are too high and causes excretion and deposition of calcium

What causes hypercalcemia?

2/3 = hyperparathyroidism 1/3 = cancers, not as common: thiazide diuretics, vitamin D overdose, infection, prolonged immobilization

clinical manifestations of hypercalcemia?

"sedative", fatigue, lethargy, weakness, confusion, hallucinations, seizures, coma, increased BP, heart block, ventricular dysrhythmias

How do we treat hypercalcemia?

Mild: low calcium diet, increase weight bearing exercise, stop and medication causing hypercalcemia Severe: isotonic IV saline, Bisphosphonates (gold standard), calcitonin

What causes hypocalcemia?

decreased production of PTH, blood transfusions, vitamin D deficiency, chronic alcohol use

Clinical manifestations of hypocalcemia?

increased nerve excitability, tetany, Trousseau's or Chvostek's sign, decreased BP, dysphagia, laryngeal stridor, circumoral numbness, VTach

What is Chvostek's sign?

Push the cheek and it spasms (mouth twitch and eye wink)

What is Trousseau's sign?

BP cuff inflated and causes a carpal spasm.

fingers flex and wrist moves in

How do we treat hypocalcemia?

mild: high calcium and vitamin D diet symptomatic: IV calcium gluconate

What do we do when giving IV calcium gluconate

treat pain and anxiety to prevent hyperventilation induced respiratory alkalosis

Range for phosphate?

2.5-4.5 mg/dL

What causes hyperphosphatemia?

kidney disease

clinical manifestations of hyperphosphatemia

similar to hypocalcemia, tetany, muscle cramps, Calcium phosphate precipitates in the skin, soft tissue, cornea, and blood vessels

How do we treat hyperphosphatemia?

-Identify and treat underlying cause

-Restrict fluids and foods high in phosphorus

-Administer oral phosphate-binding agents (calcium-carbonate

-Hemodialysis, volume expansion, and loop

diuretics for SEVERE

What causes hypophosphatemia?

decreased intestinal absorption, increased urinary excretion, or ECF to ICF shifts

clinical manifestations of hypophosphatemia?

CNS depression, muscle weakness, pain, respiratory failure and heart failure, similar to hypercalcemia

How do we treat hypophosphatemia?

Oral intake of dairy products or phosphate supplements

◦ Severe hypophosphatemia (can be fatal): IV administration of sodium phosphate or potassium phosphate, Monitor serum calcium and phosphate levels every 6 to 12 hours

Normal range for magnesium

1.3-2.1 mEq/L

What causes hypermagnesmia?

increased magnesium intake along with renal disease

Clinical manifestations of hypermagnesemia?

hypotension, facial flushing, lethargy, urinary retention, decreased deep tendon reflexes, muscle paralysis, coma

how do we treat hypermagnesemia?

stop magnesium containing drugs and dietary intake, fluids and diuretics if not contraindicated, severe: IV calcium gluconate

what is the cause of hypomagnesemia?

limited magnesium intake or increased GI/renal losses

clinical manifestations of hypomagnesemia?

Confusion, seizures, cramps, tremors, hyperactive deep tendon reflexes, and dysrhythmias such as torsades de pointes and ventricular fibrillation.

How do we treat hypomagnesemia?

oral supplements and increased dietary intake Severe: IV magnesium sulfate

What do we need to do when giving IV magnesium sulfate?

Always use an infusion pump

◦ Monitor vital signs, level of consciousness, and reflexes frequently

◦ Rapid administration can lead to hypotension and cardiac/respiratory arrest

◦ Keep IV calcium gluconate available.